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Skeletal muscle is the most abudant tissue of the human body, making up to 40 to 50% of the human body mass. While the importance of optimal muscle function is well recognized in the athletic field, its significance for general health is often underappreciated. In fact, the evidence that muscle mass, strength and metabolism are essential for our overall health is overwhelming. As the largest protein reservoir in the human body, muscles are essential in the acute response to critical illness such as sepsis, advanced cancer, and traumatic injury. Loss of skeletal muscle mass has also been associated with weakness, fatigue, insulin resistance, falls, fractures, frailty, disability, several chronic diseases and death. As a consequence, maintaining skeletal muscle mass, strength and metabolism throughout the lifespan is critical to the maintenance of whole body health. Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology, including for instance energy supply, reactive oxygen species production, calcium homeostasis and the regulation of apoptosis. It is therefore not surprising that mitochondrial dysfunction has been implicated in a large number of adverse events/conditions and pathologies affecting skeletal muscle health. While the importance of normal mitochondrial function is well recognized for muscle physiology, there are important aspects of mitochondrial biology that are still poorly understood. These include mitochondrial dynamics (fusion and fission processes), morphology and processes involved in mitochondrial quality control (mitophagy). Defining the mechanisms regulating these different aspects of mitochondrial biology, their importance for muscle physiology, as well as the interrelations will be critical for expanding understanding of the role played by mitochondria in skeletal muscle physiology and health. The present research topic provides readers with novel experimental approaches, knowledge, hypotheses and findings related to all aspects of mitochondrial biology in healthy and diseased muscle cells.Skeletal muscle is the most abudant tissue of the human body, making up to 40 to 50% of the human body mass. While the importance of optimal muscle function is well recognized in the athletic field, its significance for general health is often underappreciated. In fact, the evidence that muscle mass, strength and metabolism are essential for our overall health is overwhelming. As the largest protein reservoir in the human body, muscles are essential in the acute response to critical illness such as sepsis, advanced cancer, and traumatic injury. Loss of skeletal muscle mass has also been associated with weakness, fatigue, insulin resistance, falls, fractures, frailty, disability, several chronic diseases and death. As a consequence, maintaining skeletal muscle mass, strength and metabolism throughout the lifespan is critical to the maintenance of whole body health. Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology, including for instance energy supply, reactive oxygen species production, calcium homeostasis and the regulation of apoptosis. It is therefore not surprising that mitochondrial dysfunction has been implicated in a large number of adverse events/conditions and pathologies affecting skeletal muscle health. While the importance of normal mitochondrial function is well recognized for muscle physiology, there are important aspects of mitochondrial biology that are still poorly understood. These include mitochondrial dynamics (fusion and fission processes), morphology and processes involved in mitochondrial quality control (mitophagy). Defining the mechanisms regulating these different aspects of mitochondrial biology, their importance for muscle physiology, as well as the interrelations will be critical for expanding understanding of the role played by mitochondria in skeletal muscle physiology and health. The present research topic provides readers with novel experimental approaches, knowledge, hypotheses and findings related to all aspects of mitochondrial biology in healthy and diseased muscle cells.

Atrophy --- Mitochondria --- mitophagy --- nutrition --- Aging --- muscle contractility --- skeletal muscle --- Metabolism --- Hypertrophy --- mitochondrial dynamics

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Mitochondria play an increasingly central role in the context of cellular physiology. These organelles possess their own genome (mtDNA), which is functionally coordinated with the nuclear genome. Mitochondrial gene expression is mediated by molecular processes (replication, transcription, translation, and assembly of respiratory chain complexes) that all take place within the mitochondria. Several aspects of mtDNA expression have already been well characterized, but many more either are under debate or have yet to be discovered. Understanding the molecular processes occurring in mitochondria also has clinical relevance. Dysfunctions affecting these important metabolic ‘hubs’ are associated with a whole range of severe disorders, known as mitochondrial diseases. In recent years, significant progress has been made to understand the pathogenic mechanisms underlying mitochondrial dysfunction; however, to date, mitochondrial diseases are complex genetic disorders without any effective therapy. Current therapeutic strategies and clinical trials are aimed at mitigating clinical manifestations and slowing the disease progression to improve the quality of life of patients. The goal of the Special Issue ‘Mitochondria: from Physiology to Pathology’ published in Life (ISSN: 2075-1729) was to collect research and review articles covering the physiological and pathological aspects related to mtDNA maintenance and gene expression, mitochondrial biogenesis, protein import, organelle metabolism, and quality control.

Research & information: general --- atherosclerosis --- carotid intima-media thickness --- mitochondrial mutations --- cardiovascular risk factors --- mitochondria --- mtDNA --- cristae --- mitochondrial fission --- mitochondrial fusion --- mitochondrial diseas --- mitochondrial dynamics --- mitoenergetics --- mitosteroidogenesis --- LH --- cAMP --- Leydig cell --- mitochondrial DNA segregation --- heteroplasmy --- selective elimination --- mitophagy --- mitochondrial engineered nucleases --- kinases --- phosphorylation --- disease --- PINK1 --- Parkinson’s disease --- mitochondria homeostasis --- Cterm --- MELAS --- transmitochondrial cybrids --- aminoacyl-tRNA synthetases --- LARS2 --- mitochondrial disease --- therapeutic peptides --- FAD synthase --- FAD1 --- mitochondria localization --- Saccharomyces cerevisiae --- mRNA --- mitochondrial localization motif --- n/a --- Parkinson's disease

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Mitochondria play an increasingly central role in the context of cellular physiology. These organelles possess their own genome (mtDNA), which is functionally coordinated with the nuclear genome. Mitochondrial gene expression is mediated by molecular processes (replication, transcription, translation, and assembly of respiratory chain complexes) that all take place within the mitochondria. Several aspects of mtDNA expression have already been well characterized, but many more either are under debate or have yet to be discovered. Understanding the molecular processes occurring in mitochondria also has clinical relevance. Dysfunctions affecting these important metabolic ‘hubs’ are associated with a whole range of severe disorders, known as mitochondrial diseases. In recent years, significant progress has been made to understand the pathogenic mechanisms underlying mitochondrial dysfunction; however, to date, mitochondrial diseases are complex genetic disorders without any effective therapy. Current therapeutic strategies and clinical trials are aimed at mitigating clinical manifestations and slowing the disease progression to improve the quality of life of patients. The goal of the Special Issue ‘Mitochondria: from Physiology to Pathology’ published in Life (ISSN: 2075-1729) was to collect research and review articles covering the physiological and pathological aspects related to mtDNA maintenance and gene expression, mitochondrial biogenesis, protein import, organelle metabolism, and quality control.

Research & information: general --- atherosclerosis --- carotid intima-media thickness --- mitochondrial mutations --- cardiovascular risk factors --- mitochondria --- mtDNA --- cristae --- mitochondrial fission --- mitochondrial fusion --- mitochondrial diseas --- mitochondrial dynamics --- mitoenergetics --- mitosteroidogenesis --- LH --- cAMP --- Leydig cell --- mitochondrial DNA segregation --- heteroplasmy --- selective elimination --- mitophagy --- mitochondrial engineered nucleases --- kinases --- phosphorylation --- disease --- PINK1 --- Parkinson's disease --- mitochondria homeostasis --- Cterm --- MELAS --- transmitochondrial cybrids --- aminoacyl-tRNA synthetases --- LARS2 --- mitochondrial disease --- therapeutic peptides --- FAD synthase --- FAD1 --- mitochondria localization --- Saccharomyces cerevisiae --- mRNA --- mitochondrial localization motif

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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.

diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a

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The endometrium has been the subject of intense research in a variety of clinical settings, because of its importance in the reproductive process and its role in women's health. In the past 15 years, significant efforts have been invested in defining the molecular phenotype of the receptive phase endometrium as well as of various endometrial pathologies. Although this has generated a wealth of information on the molecular landscape of human endometrium, there is a need to complement this information in light of the novel methodologies and innovative technical approaches. The focus of this International Journal of Molecular Sciences Special Issue is on molecular and cellular mechanisms of endometrium and endometrium-related disorders. The progress made in the molecular actions of steroids, in the metabolism of steroids and intracrinology, in endometrial intracellular pathways, in stem cells biology, as well as in the molecular alterations underlying endometrium-related pathologies has been the focus of the reviews and papers included.]

endometrial stromal cells --- endometrial cell --- uterine cancer --- regeneration --- stem cell markers --- RANK --- chronic endometritis --- small RNA sequencing --- HOXA10 --- Vitamin D --- PPP2R1A --- molecular marker --- translational research --- angiogenesis --- endometriosis --- oestradiol --- mtDNA mutations --- antioxidant response --- protein phosphatase --- SMAP --- circulating tumour cells (CTCs) --- circulating tumour DNA (ctDNA) --- estrogen dependent --- endometrial regeneration --- mesenchymal stem cells --- endometrial cancer --- niche --- gene expression --- phosphoinositide 3-kinase --- lncRNAs --- mitochondrial biogenesis --- inflammation --- preclinical studies --- miRNA --- orthoxenograft --- tight junction --- proliferation --- aromatase --- testosterone --- CRISPR/Cas9 --- endometrium --- developmental pathway --- PP2A --- avatar --- infertility --- prognosis --- gene editing --- kinase inhibitor --- implantation --- haploinsufficiency --- contrast-enhanced CT scan --- pathway --- dehydroepiandrosterone (DHEA) --- CTCF --- PIK3CB --- zinc finger --- ectopic stroma --- liquid biopsy --- type II endometrial carcinoma --- eutopic and ectopic endometrium --- preclinical models --- EDN1 --- uterine aspirate --- cell contacts --- tumour suppressor gene --- pathogenomics --- mitochondrial dynamics --- adult stem cells --- PIK3CA --- murine models --- menstrual cycle --- immunomodulation --- decidualisation --- breakdown --- bioluminescence imaging --- protein kinase --- macrophages --- adherens junction --- exosomes --- immunohistochemistry --- orthotopic xenograft model --- decidualization --- p110? --- deficit of complex I --- targeted therapy --- mesenchymal stem cell --- sulfatase --- TRP channels --- personalized medicine --- mitophagy --- miR-375 --- migration --- microRNA --- gap junction --- cancer --- LGR5 --- miR-139-5p